Furthermore, PARK2 levels were decreased in lung homogenates from COPD patients, and there was a positive correlation between PARK2 levels and percentage of FEV1/FVC of pulmonary function test, suggesting the causal link between insufficient PARK2-mediated mitophagy and airway obstruction associated with accelerated cellular senescence during COPD pathogenesis. Here, PRKN is linked to chronic obstructive pulmonary disease.